title: Metabolism of malonaldehyde in vivo and in vitro.
abstract: The metabolism of malonaldehyde (MA) was investigated in vivo using male Wistar rats and in vitro using rat liver mitochondria. Twelve hr after intubation with [1,3-14C] MA, 60-70%, 5-15% and 9-17% of administered radioactivity was recovered in expired CO2, feces and urine, respectively. In rats intubated with [1,2-14C) acetate, the corresponding values were 68-82%, 1-2% and 2.3%. 14CO2 evolution was initially slower after 14C-MA administration than after 14C-acetate administration and more radioactivity was excreted in the feces and urine. In vitro experiments using [1,3-14C] MA showed that MA is metabolized primarily in the mitochondria via reactions involving O2 utilization and 14CO2 production. The apparent Km and Vmax were 0.5 mM and 9.3 nmol/min/mg protein for O2 uptake, respectively, and 2.0 mM and 2.4 nmol/min/mg protein for 14CO2 production. Addition of malonic acid to mitochondrial incubates at concentrations inhibitory to succinate dehydrogenase did not affect MA-induced O2 uptake but enhanced 14CO2 production from 14C-MA. 14C-Acetate appeared to be the major accumulating metabolite in rat liver mitochondrial preparations following a 120-min incubation with 14C-MA. A probable biochemical route for MA metabolism involves oxidation of MA by mitochondrial aldehyde dehydrogenase followed by decarboxylation to produce CO2 and acetate.
mesh_terms: D000085:Acetates / Q000378:metabolism; D000818:Animals; D002245:Carbon Dioxide / Q000378:metabolism; D007700:Kinetics; D008297:Male; D008314:Malonates / Q000378:metabolism*; D008315:Malondialdehyde / Q000378:metabolism*; D008930:Mitochondria, Liver / Q000378:metabolism; D008956:Models, Chemical; D010101:Oxygen Consumption; D051381:Rats; D011919:Rats, Inbred Strains; D013385:Succinate Dehydrogenase / Q000378:metabolism; D013997:Time Factors
chemical_list: D000085:Acetates; D008314:Malonates; D002245:Carbon Dioxide; D008315:Malondialdehyde; D013385:Succinate Dehydrogenase